SPEAKER_01: 0:00

Welcome back to the deep dive. Today we are tackling an absolutely essential topic in gastroenterology, something that is uh just fundamental for clinical practice, inflammatory bowel disease. We're going to be getting into Crohn disease and ulcerative colitis. And our mission today, it's not just about reciting facts. We've really tried to distill the core knowledge you need to, well, to quickly tell them apart, get the diagnosis right, and then confidently manage these really complex diseases.

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And I think that's the perfect way to frame it.

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It's about the why, not just the what.

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Yes. Because you can't just lump IBD together. You have to start by stressing that Crohn disease or CD and ulcerative colitis, you see, are just fundamentally distinct processes. They just, you know, happen to share the same neighborhood in the GI tract.

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Trevor Burrus, Jr.: So let's start right there with the foundational concepts, the uh the basic architecture of the inflammation.

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Aaron Powell Okay, so think of the bowel wall as having multiple layers. Ucerative colitis is, well, it's restricted. It's a diffuse inflammation, but it only affects that inner lining, the mucosa.

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Just the surface.

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Just the surface. And it's confined to the colon. Crucially, it almost always starts in the rectum and then just extends upwards in a continuous, uh unbroken fashion.

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Aaron Powell So like peeling the wallpaper off a room, it's just that top layer.

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Aaron Powell That's a great analogy. But Crohn's disease, well, that's different. It's far more aggressive. It's transmural. Meaning it goes through all the layers of the bowel wall from the inner mucosa right through to the outer layer. And it can affect any part of the GI tract, mouth to anus.

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And it has that classic signature.

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The classic signature skip lesions. You get these segments of really inflamed bowel, separated by stretches of perfectly normal, healthy tissue. It jumps around.

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Okay, so that distinction transmural and segmental for Crohn's versus mucosal and continuous for UC, that's the foundation for everything else.

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It is.

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But then you have this really counterintuitive risk factor, the smoking paradox.

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Aaron Powell It's one of the most surprising things in chronic disease, honestly. For Crohn disease, smoking is just bad. It's strongly associated with getting the disease, having worse flares, and you know, needing more surgery.

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Aaron Powell But for UC, it's the complete opposite.

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Aaron Powell Precisely. Ulcerative colitis is actually more common in people who don't smoke or who have quit. And here's the wild part patients with UC will often tell you their disease got much worse after they quit smoking.

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Aaron Powell Which is not a reason to start smoking, obviously.

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Of course not. But it just highlights this fundamental, you know, unresolved difference in what's actually driving these two diseases. Trevor Burrus, Jr.

SPEAKER_01: 2:31

That is a fantastic clinical pearl. Okay, let's pivot now to the clinic. History taking and physical examination. This is where we really start to sort them out.

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Your history is your sharpest tool right at the start. For ulcerative colitis, the story is often really dramatic. The hallmark is bloody diarrhea. And it's typically frequent small volume stools with blood and mucus. You'll also hear about lower abdominal cramps that feel better after a bowel movement, urgency, and tenes. That painful, incomplete sensation, yes. So if you hear bloody diarrhea and tenes, your brain should be screaming UC.

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And how does that picture change for Crohn's?

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Crohn's is often more um insidious, more subtle. Patients will describe an intermittent low-grade fever, just feeling unwell, losing weight without trying. And the pain is often focal, usually in that right lower quadrant.

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The RLTLQ, because that's where the terminal alleleum is?

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Exactly, the most common spot for Crohn's. And the diarrhea is common, but it's typically non-bloody.

SPEAKER_01: 3:36

Ah, but that can be a trap, right?

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It can be a huge trap. Because if Crohn's involves the colon, you can absolutely get bloody diarrhea. One other clue though, if a patient tells you they get cramping pain specifically after they eat, that should make you think about intestinal stretching from the disease. That's a great detail.

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All right, moving on to the physical exam. Beyond just checking their vital signs, what are the specific findings that point you one way or the other?

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Well, the exam is non-negotiable, especially for finding complications. For Crohn's, you're going to feel for that focal tenderness, usually RLQ or maybe even a lipable mass.

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A mass? What is that?

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It's those severely thickened, inflamed loops of bowel all matted together. But the single most critical thing you have to do is the perianal exam.

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Why is that so vital for Crohn's?

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Because it's a direct reflection of that transmural inflammation we talked about. The disease tunnels through the whole bowel wall. So about a third of patients will have, you know, fissures, deep abscesses, complex fissulose, or these big skin tags around the anus.

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And finding that is almost diagnostic.

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It's almost pathognomonic for Crohn's. You just don't see that with UC.

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Okay, so for UC, what are the big red flags on an exam?

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For UC, you might find some general tenderness, but what you're really looking for is abdominal distension. A tense, quiet abdomen is a massive red flag for toxic megacolon. That's a surgical emergency.

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And we can't forget the extraintestinal manifestations, the EIMs.

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Absolutely not. They happen in both, and you have to ask about them. Oral ulcers, joint pain, especially in the spine, red painful eyes from uveitis, skin changes.

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Like erythema nodosum.

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Exactly, those tender red nodules. Or pyodermogangrinosum, those nasty ulcers. If your patient has IBD and a red eye, you need to be thinking uveitis and get them to ophthalmology fast.

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Okay, so history and exam have given us a pretty strong suspicion. Now we need the data. Let's talk with them more. Using diagnostic studies and formulating a diagnosis.

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Step one is labs. You're confirming inflammation and ruling out mimics. So you'll often see anemia, which makes sense, right? Chronic inflammation, blood loss, or even B12 malabsorption if the ioleme is involved in Crohn's.

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And inflammatory markers.

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CRP is a must. C reactive protein. If it's elevated, that supports active inflammation. But, and this is a key caveat, it can be normal in about 15% of active cases.

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So what's a better marker?

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The real star here is fecal calprotectin.

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Ah, yes. Tell us why that's so useful.

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Well, calprotectin is a protein that gets released by white blood cells into the stool when there's inflammation in the gut. A high level is super sensitive for active IBD, and just as importantly, helps you differentiate it from something like IBS where there isn't that inflammation.

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And before we even think about IBD, there's a huge rule out.

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You must, must, must do stool studies to rule out infection.

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C. diff. Salmonella.

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C. diff salmonella shigella parasites. You can't diagnose a chronic disease until you've ruled out an acute infection that could look identical. Giving immunosuppressants to someone with C. diff would be a diseaster.

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Okay. Infection is cleared. Now for the definitive studies, endoscopy and imaging. What does quones look like on a scope?

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We're looking for those skip lesions, that discontinuous inflammation. The classic look is cobblestoning, where deep linear ulcers crisscross the swollen mucosa. Biopsies might show granulomas, which is a huge clue, but you don't always find them.

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And for ulcerative collitis.

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It's the opposite. It's a continuous sheet of inflammation. It starts at the rectum and just goes up. The mucosa is red, it's friable, meaning it bleeds if you just touch it with a scope, and it's covered in mucopus. But no skip lesions, no cobblestones.

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Now what about imaging? For Crohn's, we have to see the small bowel, right?

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Correct. So we use CT or MR anterography. We're looking for wall thickening, strictures, fistulas, and that sign you mentioned before, fat stranding.

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Let's break that down. What is fat stranding?

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So on the scan, the fat around the bowel should look black and clean. Fat stranding is when that fat looks hazy, gray, and streaky. It means the inflammation is so bad it's leaking out of the bowel and into the surrounding tissue. It's a direct sign of that transmural process in Crohn's.

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And we can't forget the simple abdominal X-ray.

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Never. In a sick UC patient, you get a plain film to look for toxic megacolon. You'll see the colon blown up to more than six centimeters.

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All right, so we've ruled out infection, we've looked at the other mimics like ischemic colitis or microscopic colitis.

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Which is that one with watery diarrhea and a normal-looking scope, right?

SPEAKER_01: 8:07

Exactly. Diagnosis is only on biopsy. So once all that work is done, we can make the call. CD is confirmed by segmental disease, UC by continuous disease from the rectum up. Right. Now we can talk about managing patients and pharmaceutical therapeutics.

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The management is always a step-up approach. Start with the mildest effective drugs.

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Which would be the amanosolicillates or five ASAs.

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Exactly. These are first line from mild to moderate ulcerative colitis. And a key point here is that topical versions, suppositories, enemas, are often much better for distal disease because you're putting the medicine right where the problem is. Their role in Crohn's, though, is pretty limited.

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Okay, next step up. And here comes the big steroid warning.

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This is so, so important. Corticosteroids, like prednisone, are fantastic for inducing remission, for putting out a fire during a flare. But they are absolutely not for maintenance therapy.

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Because the long-term risks are just too high.

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Way too high. Osteoporosis infections, cataracts. This is a long and scary list. But there's a specific steroid for Crohn's, but mild to moderate Crohn's in the oleum. It has a high first pass metabolism, meaning the liver inactivates it very quickly after it does its job in the gut. So you get far fewer of those systemic side effects. But again, it's for induction, not maintenance.

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So to get people off steroids and keep them in remission, we move to the immunomodulators.

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Correct. The thiopurines, like azatheoprine. They are great steroid-sparing agents. But here is the absolute must-know safety check. Before you start one, you have to check the patient's TPMT activity.

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And what is TPMT?

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It's the enzyme that metabolizes these drugs. If a patient is deficient in that enzyme, the drill builds up to toxic levels and can cause severe life-threatening bone marrow suppression. It's a simple blood test that you have to do first.

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And for patients who can't take those or for more severe disease, we have the biologics and small molecules.

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Which are now really the standard of care for moderate to severe IBD. You have the anti-TNF agents like infliximab. You have newer, more targeted drugs like Vatalizomap, which is an anti-indocrine that works specifically in the gut.

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Less systemic immunosuppression.

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Potentially, yes. And then you have the oral agents, the JK inhibitors.

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Like tofacotina.

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Right. They're convenient because they're a pill, but they come with a major black box warning for blood clots, heart problems. So it's a serious conversation you have to have with the patient about risks and benefits.

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That covers the meds. Let's move to clinical intervention and health maintenance. This is where the paths of C D and UC really, really diverge.

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They do. Let's start with nutrition. Patients with Crohn's affecting their ilium often need B12 shots because that's where it's absorbed. And anyone who's been on steroids needs vitamin D and calcium for their bones.

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Now for the biggest difference of all, surgery.

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This is the ultimate distinction. For Crohn disease, surgery is never curative. Can't be. We only operate for complications, an obstruction, an abscess, a fistula. And sadly, the disease almost always comes back, usually right near where the surgeon reconnected the bowel.

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Just a devastating reality for those patients.

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It is. Over half will need at least one surgery.

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But compare that to UC.

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With ulcerative colitis, surgery is curative. But total proctocolctomy, removing the entire colon and rectum, cures the disease. The disease is gone.

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When would you do that?

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For a massive bleed, for toxic megacolon, for cancer, or if the disease just doesn't respond to any medical therapy. It's a major operation, but it is a cure.

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And for that hospitalized patient with severe colitis, what's the protocol?

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Aggressive. Make them NPO, give IV fluids and high dose IV steroids. And you reassess in three to four days. If they're not clearly better, you have to escalate. Move to salvage therapy like infliximab, or if they're really sick, you move to surgery. You can't wait.

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Okay, let's wrap up with the long game. Health maintenance, patient education, and prevention.

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This is crucial. Because of the chronic inflammation, there's a higher risk of colorectal cancer. So surveillance colonoscopy has to start eight years after the initial diagnosis for anyone with colitis.

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Eight years. That's a key number.

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It's a non-negotiable number. And because of the medications, there are other risks. Annual skin checks for skin cancer, routine cervical screening.

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And the big one for patient education. Vaccinations.

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A critical safety talk. Inactivated vaccines like the flu shot, pneumococcal, shingrix, they're all safe and recommended. But live vaccines, MMR, Varicella, are absolutely contraindicated for anyone on significant immunosuppression. A live vaccine could cause a serious infection in them.

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So we've spent this deep dive differentiating everything from the pathology to the management.

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We have.

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And that one difference drives everything.

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It dictates every single clinical decision we make.

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So as we finish up, what's the final thought for the clinician out there trying to build a long-term plan for these patients?

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Well, it leaves you with a question to reflect on. While our drugs are getting better and better for both conditions, think about the finality of the interventions. UC has a definitive surgical cure. You can remove the organ and the disease is gone. Crohn's, on the other hand, is a lifelong systemic, unpredictable process. So how does that profound difference in curability change your conversation, your long term goals, and even the psychological support you offer a patient when they first receive that diagnosis?